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Exploring the effects of LIN28B on receptor editing and B-cell differentiation

Sundberg, Angelina (2025) MOBN03 20242
Degree Projects in Molecular Biology
Popular Abstract
Can Lin28b treat childhood leukemia?

B-cell precursor acute lymphoblastic leukemia (BCP-ALL) is one of the more common types of cancer in children. This disease originates mainly from progenitors of a white blood cell type known as the B-cell. Mature B-cells are mainly known for helping us clear infections by producing pathogen-binding antibodies. Because BCP-ALL cancer cells stem from B-cell precursors, studying their differentiation is crucial for finding potential therapeutic targets of the condition.

The origin of a wide range of unique antibodies begins during B-cell differentiation. As the B-cell progenitor differentiates, it develops a B-cell receptor, a cell surface-bound precursor of free antibodies. The uniqueness of the... (More)
Can Lin28b treat childhood leukemia?

B-cell precursor acute lymphoblastic leukemia (BCP-ALL) is one of the more common types of cancer in children. This disease originates mainly from progenitors of a white blood cell type known as the B-cell. Mature B-cells are mainly known for helping us clear infections by producing pathogen-binding antibodies. Because BCP-ALL cancer cells stem from B-cell precursors, studying their differentiation is crucial for finding potential therapeutic targets of the condition.

The origin of a wide range of unique antibodies begins during B-cell differentiation. As the B-cell progenitor differentiates, it develops a B-cell receptor, a cell surface-bound precursor of free antibodies. The uniqueness of the B-cell receptor binding capacity is formed as the cell rearranges its own DNA. If the B-cell receptor is reactive against the body’s own tissues, the B-cell precursor may under later stages of development rearrange its DNA again.

BCP-ALL cancer cells stem mostly from differentiation blocks at B-cell progenitor stages, likely since their ability to edit their own DNA confers risk of mutagenesis, in combination with their high rates of cell division. Since levels of B-cell differentiation are much higher during early life stages, so is the risk of developing BCP-ALL. The disease can be studied using mouse models that display a differentiation block at B-cell progenitor stages and an increased risk of developing the cancer especially in combination with other genetic predispositions.

Lin28b is a protein which is naturally expressed in B-cell progenitors of early life in both human and mouse. We addressed LIN28B’s effects on B-cell differentiation, and its interactions with the cancer predisposing factors. We compared critical steps in B-cell differentiation to understand the mechanism of action of LIN28B. To assess the protein’s effects on B-cell differentiation in BCP-ALL models, we used viral vectors that integrate an active Lin28b gene into the DNA of cells. We isolated B-cell progenitors from mouse models of ALL and infected them with the viruses. However, we did not observe the expected differentiation block nor any effects of LIN28B on B-cell differentiation, indicating that the method did not work well. Although no conclusions could be drawn from these data, the hypotheses still remain. If LIN28B in the future is revealed to affect the BCP-predisposing traits of leukemia models, this could reveal new drug targets for treating the disease.


Master’s Degree Project in Molecular Biology, 60 credits, 2025
Department of Biology, Lund University

Advisor: Joan Yuan
Department of Laboratory Medicine (Less)
Please use this url to cite or link to this publication:
author
Sundberg, Angelina
supervisor
organization
course
MOBN03 20242
year
type
H2 - Master's Degree (Two Years)
subject
language
English
id
9214820
date added to LUP
2025-11-03 15:10:45
date last changed
2025-11-03 15:10:45
@misc{9214820,
  author       = {{Sundberg, Angelina}},
  language     = {{eng}},
  note         = {{Student Paper}},
  title        = {{Exploring the effects of LIN28B on receptor editing and B-cell differentiation}},
  year         = {{2025}},
}